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A Pacing-Controlled Procedure for the Assessment of Heart Rate-Dependent Diastolic Functions in Murine Heart Failure Models
Published on: July 21, 2023
Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction
Paul S Bhella1, Anand Prasad, Katja Heinicke
1The Institute for Exercise and Environmental Medicine, 7232 Greenville Avenue, Dallas, TX 75231, USA.
Peak oxygen uptake is reduced in heart failure with preserved ejection fraction (HFpEF) patients, but cardiac reserve is not impaired. An abnormal exercise response suggests impaired skeletal muscle metabolism may limit functional capacity in HFpEF.
Area of Science:
- Cardiology
- Exercise Physiology
- Metabolic Research
Background:
- Patients with heart failure with preserved ejection fraction (HFpEF) exhibit reduced peak oxygen uptake (VO(2)), suggesting compromised cardiac reserve.
- Assessing the hemodynamic response to exercise is crucial for understanding functional limitations in HFpEF.
Purpose of the Study:
- To investigate the hemodynamic response to exercise in patients with HFpEF.
- To determine if cardiac reserve is impaired in HFpEF patients.
Main Methods:
- Compared exercise hemodynamics (cardiac output, VO(2)) in 11 HFpEF patients and 13 healthy controls.
- Measured cardiac output (Q(c)) using acetylene rebreathing during graded exercise.
- Determined peak oxygen uptake (VO(2)) using Douglas bags.
Main Results:
- HFpEF patients had significantly lower peak VO(2) compared to controls (13.7 ± 3.4 vs. 21.6 ± 3.6 mL/kg/min).
- Peak cardiac power output and stroke work were not significantly different between groups, indicating preserved cardiac reserve.
- The ratio of change in cardiac output to change in VO(2) (ΔQ(c)/ΔVO(2)) was significantly higher in HFpEF patients (11.2 ± 3.6 vs. 8.3 ± 1.5).
Conclusions:
- Cardiac reserve is not significantly impaired in well-compensated HFpEF outpatients.
- The abnormal exercise response in HFpEF, characterized by reduced peak VO(2) and an increased ΔQ(c)/ΔVO(2) slope, suggests impaired skeletal muscle oxidative metabolism.
- This skeletal muscle impairment may contribute to reduced functional capacity through premature fatigue and exaggerated metabolic signals for cardiac output, potentially stressing a diastolic-impaired left ventricle.
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